We chose to use glioblastoma cells because: (i) a characteristic splicing switch from PK-M1 to PK-M2 occurs during gliomagenesis [6,20]; and (ii) glioblastoma cell lines have a higher basal level of PK-M1 mRNA, which we expected to facilitate the ASO-mediated PK-M splicing switch [6]. This evidence concerns the gene PKM and glioblastoma.